慢性哮喘气道重建的研究

To explore the effect of changing the mechanical parameter on airway structure and function in rat asthma model； to analysis the characteristics of airway remodeling at different phase in asthma process; at the same time, to observe the effect of lung diffusing therapy, body resistance-strengthening therapy, ntegrated therapy both of them as well as routine therapy of western medicine on airway remodeling in these at asthma models, in order to find effective method to prevent the development of airway inflammation and airway remodeling..Methods: Three groups were divided randomly in the experiment. 1.e. normal group、 asthma model groups （ inducing asthma 15d, 30d, 45d, and 60d respectively）and Treating group.Mechanical character of trachea of all rats were examined using air passage mechanical test device.Levels of cytokines in all rat serums were tested through ELISA methods. At the same time, changes of fibrinectin and collagenous fibers in trachea and pulmonary tissues were observed through immunology. The pathological changes in pulmonary tissue were observed through pathologic staining method.Result:(1) the opening angles and residual strains of the normal rat trachea: After analyzing no-load state and zero-stress state of the normol rat trachea,We find that there exist compressive residual strains at inner wall region of the rat trachea and tensile residual strain at outer wall region.The fact that the opening angles cut at the midpoint of the cartilaginous region is significantly larger than that cut at the muscular portion shows that residual strains exist mainly in the muscular region in the rat trachea.It was also indicated that the opening angles and residual strains expressed by cutting at the muscular portion are basically identical along longitudinal location and those expressed by cutting in the cartilaginous region tend to increase in the longitudinal direction in the normal rat,and that there exists quantitatively positive correlation between the opening angles and residual strains in rat trachea. (2) The remodeling characteristic of asthma model rat airway remodeling: The opening angles and circumferential residual strains of the model rat is significantly larger than the normal rat（p<0.05）; as the normal group, there exists obvious difference among the tracheal sectors from cartilaginous cut and those from muscular cut: the tracheal sectors from muscular cut are horseshoe-shaped and the corresponding opening angles are relatively small and quite uniform in axial direction; whereas the opening angles of the sectors of cartilaginous cut are relatively large and vary significantly along the tracheal axes. The farther away from the larynx the tracheal sector, the larger the opening angle. And the corresponding zero-stress tracheal sectors are no longer U-shaped, but more in the shape of ' '.The experiment results of the rat air passage P- V difusion manifeste that the compliance of the asthma rat trachea V0 at zero-press state significantly decreased as compared with the normal rat（p<0.05）. Ⅱ. The TNF-α, IL-4 and LTB4 of the cytokines in blood serum of modelled rats remarkably increased while IFN-γ significantly decreased. The pathological manifestations were serious submucous Eos infiltration in the lung and bronchus, hyperplasia and sedimentation of fibronectin and collagenous fibers.(3) The airway remodeling changement of different disease-phase asthma rat:Ⅰ.Along the axial direction,the opening angles of the first disease-phase modelled rat was remarkably smaller than that of the third-phase modeled rat;There were not significant difference between the opening angles of the second,third and fouth disease-phase (P>0.05). While there were not significant difference between the all residual strains of the all disease-phase rat. Ⅱ.The inner wall circumference of different disease-phase modeled rat is smaller than that of the normal rat for both cartilaginous cut and muscular cut. And similar to the nomal rat,the inner arc of tracheal sector would extend and the outer arc would shorten,t

哮喘的特征病理改变是气道壁增厚，内腔变窄，导致气道通气障碍，这也是哮喘不易根治的重要病理原因。本课题通过观测哮喘模型动物，探明哮喘病程、气道炎症对气道流量因而对气道重建的影响，揭示气道壁增厚，内腔变窄的力学机制，为探讨哮喘的发病机制，寻找控制和预防哮喘的途径提供新思路，同时也为研究机体应力－生长关系提供重要补充。..